平滑肌大电导钙激活钾通道在重症失血性休克细胞膜超极化中的作用

Role of large conductance calcium-activated potassium channel of arteriolar smooth muscle cells in cell membrane hyperpolarization after severe hemorrhagic shock

目的 探讨失血性休克后大鼠肠系膜细动脉血管平滑肌细胞膜电位和大电导钙激活钾通道 (BKCa)的变化。 方法 (1)将Wistar大鼠分为假手术组和休克组。复制失血性休克模型 ,假手术组只做手术 ,不放血 ;(2 )急性分离大鼠肠系膜A2、A3动脉 ,链霉蛋白酶法急性分离血管平滑肌细胞 ;(3)用膜片钳的细胞贴附式和内面向外式记录法记录假手术组和休克组细胞膜电位和通道的变化。 结果 (1)失血性休克 2h后血管平滑肌细胞膜电位由正常的 - 4 1mV变化为- 6 5mV ;(2 )休克后BKCa开放概率增加 ,反转电位明显改变 ,而单通道电导没有变化。 结论 失血性休克后血管平滑肌细胞膜超极化 ,BKCa活动增加可能是导致膜超极化的主要原因。

Objective To investigate the changes of membrane potential of mesenteric arteriolar smooth muscle cells (ASMCs) and large conductance calcium-activated potassium channel (BK Ca ) following hemorrhagic shock in rats. Methods (1) The Wistar rats were randomly divided into sham and shock groups. The hemorrhagic shock model was duplicated. The sham group was given operation rather than bloodletting. (2) ASMCs were isolated with pronase E and mesenteric arteries A2 and A3 from sham and shock rats also isolated. (3) The changes of membrane potential of ASMCs and potassium channel were recorded using cell-attach and inside-out patch lamps. Results (1) The membrane potential of ASMCs changed from -41 mV to -65 mV two hours after hemorrhagic shock. (2) After shock, the conductance of BK Ca did not change, while the open probability (NPo) of BK Ca was enhanced and the reversal potential of BK Ca changed significantly. Conclusions Membrane hyperpolarization of ASMCs occurs posterior to hemorrhagic shock, the cause for which may be the activation increase of BK Ca .